Linked Life Data

16638913

Source:http://linkedlifedata.com/resource/pubmed/id/16638913

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-8-10
pubmed:abstractText
Prostasin is a glycosylphosphatidylinositol-anchored serine protease, with epithelial sodium channel activation and tumor invasion suppression activities. We identified the bladder as an expression site of prostasin. In the mouse, prostasin mRNA expression was detected by reverse transcription and real-time polymerase chain reaction in the bladder, and the prostasin protein was localized by immunohistochemistry in the urothelial cells. In mice injected intraperitoneally with bacterial lipopolysaccharide (LPS), bladder prostasin mRNA expression was downregulated, whereas the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interferon-gamma (IFN-gamma), TNF-alpha, IL-1beta, and IL-6 was upregulated. Viral promoter-driven expression of the human prostasin homolog in the bladder of transgenic mice attenuated the LPS induction of iNOS but did not abolish the induction. LPS induction of COX-2, TNF-alpha, IL-1beta, and IL-6 expression, however, was not reduced by prostasin transgene expression. Liposome-mediated delivery of prostasin-expressing plasmid into mouse bladder produced similar attenuation effects on LPS-induced iNOS expression, while not affecting COX-2 or cytokine induction. Mice receiving plasmid expressing a catalytic mutant prostasin did not manifest the iNOS induction attenuation phenotype. We propose a proteolytic mechanism for prostasin to intercept cytokine signaling during LPS-induced bladder inflammation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F567-77
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:16638913-Animals, pubmed-meshheading:16638913-Cyclooxygenase 2, pubmed-meshheading:16638913-Down-Regulation, pubmed-meshheading:16638913-Humans, pubmed-meshheading:16638913-Inflammation, pubmed-meshheading:16638913-Interferon-gamma, pubmed-meshheading:16638913-Interleukin-1, pubmed-meshheading:16638913-Interleukin-6, pubmed-meshheading:16638913-Lipopolysaccharides, pubmed-meshheading:16638913-Male, pubmed-meshheading:16638913-Mice, pubmed-meshheading:16638913-Mice, Transgenic, pubmed-meshheading:16638913-Nitric Oxide Synthase Type II, pubmed-meshheading:16638913-Serine Endopeptidases, pubmed-meshheading:16638913-Tumor Necrosis Factor-alpha, pubmed-meshheading:16638913-Up-Regulation, pubmed-meshheading:16638913-Urinary Bladder Diseases, pubmed-meshheading:16638913-Urothelium
pubmed:year
2006
pubmed:articleTitle
Prostasin attenuates inducible nitric oxide synthase expression in lipopolysaccharide-induced urinary bladder inflammation.
pubmed:affiliation
Department of Molecular Biology and Microbiology, University of Central Florida, 4000 Central Florida Boulevard, Orlando, FL 32816-2364, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural